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Cementum

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INTRODUCTION: Cementum is highly specialized form of connective tissue which is hard, calcified, avascular, mesenchymal tissue and forms outer covering of anatomic roots of teeth. It was first described way back in 1835 by two pupils of Purkinjee and yet until recently has remained a poorly defined tissue both at the cellular and molecular level. Cementum furnishes a medium for attachment of collagen fibers that bind the tooth to the surrounding structures. Root cementum has important adaptive and reparative functions. Light & electron microscopy revealed several varieties of cementum. It forms the interface between root dentin & the periodontal ligament. Cementum is unique in that it is avascular, no innervations, no direct blood supply & no lymph drainage. It does not undergo continuous remodeling like bone but continuous to grow in thickness throughout the life. The ultimate goal of true periodontal ligament after treatment for periodontitis has revived great interest in this unique tissue. It is necessary to know about the normal and diseased cementum for careful evaluation of agents that are being marketed for their abillity to regenerate periodontal tissues

specially the agents for cementum regeneration. Hence the aim of this seminar is to provide a comprehensive insight into cementogenesis, its physical & chemical properties, its structural composition and various conditions, both systemic as well as local, that lead to changes in cementum & current concepts in periodontal regeneration.

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DEVELOPMENT OF CEMENTUM {CEMENTOGENESIS}: The formation of cementum can be subdivided into prefunctional & functional development stage. Prefunctional portion of cementum is formed during root development. Functional development of cementum takes place when tooth is about to reach occlusal level, is associated of the root to the surrounding bone and continuous throughout the life. PREFUNCTIONAL: Cementum formation in developing teeth is preceded by deposition of dentin along the inner aspect of hertwig¶s epithelial root sheath (HERS). Once the first layer of radicular mantle dentin has been laid down by maturing odontoblasts and before mineralization of dentin reaches the inner epithelial cells, HERS is fragmented. Cells from the dental follicle then penetrate the HERS and occupy the area next to the predentin. This direct contact of dentin with connective tissue of dental follicle, undifferentiated ectomesenchymal cells differentiate into cementoblasts and begin to produce collagen fibers at right angles to the surface. The first cementum is deposited on the superficial layer of mantle dentin called the hyaline layer which contains enamel matrix proteins and initial collagen fibers of the cementum which takes their origin from cells of the dental follicle and later from the newly differentiated cementoblasts. Subsequently cementoblasts drift away from the surface resulting in increased thickness of the cementum & incorporation of principle fibers.

PRECEMENTUM (CEMENTOID): Precementum is the outermost layer of cemental matrix which persists for life of the tooth. It is unmineralised tissue& begins initially at the cemento-enmel junction. It is located between calcified layer and cementogenic or cementoblastic layer. The width of this layer is about 3- 5 µm thick, further apically it may be about a micron thick. In H & E staining this layer is highly refractile & eosinophillic. Cementoid provides a compatible environment for cementoblasts and serves a protective function by preventing cementum resorption and attach the tooth to surrounding bone.

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. On dry weight basis. 2. on the basis of visual examination alone. glycoproteins & phosphoporteins. With age permeasibility of cementum diminishes (Blayney JR et al 1941). where compensates for tooth eruption which itself compensates for attrition. Permeability of Cementum: Cellular and Acellular cementum are permeable to variety of materials. ORGANIC MATERIAL (50-55%): Organic portion of cementum consists primarily of type I collagen. COLLAGEN: The collagen is composed of three polypeptide alpha attached to each other to form classic triple helix configuration. Cementum is the highly calcified connective tissue that covers the root surface of the teeth from the cemento-enamel junction to the apex and also lines the apex of the root canal. it
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COMPOSITION OF CEMENTUM: Biochemical studies have shown that the composition of cementum is similar to that of bome. which makes it difficult to distinguish between two. Cementum formation is most rapid in apical regions. 4. I.PHYSICAL CHARACTERISTICS OF CEMENTUM: 1. constituting upto 90% of the matrix and protein polysaccherides(proteoglycans). cementum has 45-50% inorganic substances & 50-55% organic material and water. In the cellular cementum the canaliculi in some areas are contiguous with the dentinal tubuli. Cementum is light yellow in colour and can be distinguished from enamel by its lack of luster & its darker hue. Hardness of the full mineralized cementum is less than that of the dentin meaning it is softer than dentin (Selwig 1962). It is the most important part of the attachment because it is the site through which the connective tissue apparatus of the periodontal ligament are inserted into the tooth. 3. The permeability of cellular cementum is greater than that of acellular cementum. 5. But it is lighter than dentin.

fibronectin & tensin are of high molecular weight & widely distributed. and play a role in cementoblast progenitor cells. are called extrinsic fibers. Type I collagen known to promote cell attachment and also a critical molecule for maintaining the integrity of both soft and hard connective tissue. Those derived from sharpey¶s fibers are embedded at right angle or oblique into root surface. proteolipids. Studies have demonstrated that type XII collagen is expressed by periodontal ligament cell during later stages of root development (Karimbux & Macneil et al). bone sialoprotein. osteopontin . Osteocalcin. They are multifunctional proteins of organic matrix. Two other glycoproteins. fibril associated collagen binds to type I collagen and also to non-collagenous proteins. VI & XIV collagen also found in mature cementum. Extrinsic fibers are responsible for tooth anchorage & are produced by fibroblasts of periodontal ligament. Trace amounts of type V. during development as well as repair. ~7~
. It has been suggested that type III collagen coat type I collagen fibrils (Wang HM et al 1979). Organic matrix either derived from sharpey¶s fibers or from cementoblasts itself. repair & regeneration and it accounts for less than 5% of the total. Type XII collagen. proteoglycans & phosphoproteins and variety of proteins like Those are found in bone viz. II. Osteonectin.. Bone sialoprotein & Osteopontin are predominant non collagenous glycoproteins proteins. dentin matrix protein-I & several growth factors including insulin like growth factor (IGF).The organic matrix of cementum consists primarily of type I collagen. ales cross linked collagen found in high concentrations during development. In contrast those derived from cementoblasts run parallel to root surface & right angle to extrinsic fibers are called intrinsic fibers. Type III collagen. NON COLLAGENOUS PROTEINS: Cementum is rich in glycocojugates which are either glycolipids. are expressed during early tooth development. takes part in mineralization process. They have cell attachment properties. They bind cells to components of extracellular matrix.glycoproteins. cementum attachment / adhesion molecule. They bind tightly to collagenous matrices & hydroxyapatite.

It is well known that protein extracts of mature cementum promote cell attachment and cell migration & stimulate protein synthesis of gingival fibroblasts & periodontal ligament cells (Somerman et al 1987). Osteocalcin is present in acellular cementum & its associated cementoblasts (Tenorio et al 1993). HYDROXYAPATITE CRYSTALS: Like in all other calcified tissues the principle component is hydroxyapatite crystals. Cementoblasts & cementocytes produce high levels of the GLUT-1 monosaccharide transporter. Some cementum specific proteins are also present such 55. Osteopontin and 55-k Da cementum attachment protein. Osteocalcin appears to be involves in mineralization process (Hauschka 1989). And CIFC and associated cementoblasts stained weekly in immunohistochemical studies. They are the aggregates of calcium & phosphate salts derived from ~8~
. Proteoglycans of cementum are small proteins. III. dermatan sulphate. Other multifunctional proteins such as laminin & fibronectin which are believed to be a chamo-attaractants. which may play a role in cementogenesis and could be serves as a biomarker to differentiate between cementoblastic & osteoblastic lineage (Koike H et al 2005). bone sialoprotein. In cellular variety acellular extrinsic fiber cementum is more mineralization because it is slowly formed which allows longer direct contact with tissue fluids.k Da CAP (Parker T et al 1996) as a mitogenic factor (Narayan S et al 1991) and 72-k Da protein. Enzyme alkaline phosphate is thought to participate in cementum mineralization (Beensten 1989). Acellular extrinsic fiber cementum is highly mineralized than other because of uncalcified spaces such as lacunae & uncalcified core of sharpey¶s fibers. hyaluronic acid. CEM-1 (Slavkin HC et al 1989). Enamel related proteins also been detected in cementum. a. as glycosoaminoglycan in cementum. They also function as adhesion proteins together with tenasin. chondroitin -6-sulphate. Osteocalcin is present on cellular intrinsic fiber cementum (CIFC) and associated cementoblasts (Bronkers et al 1994) but not in acellular cementum & associated cementoblasts. INORGANIC MATERIAL (45-50%): Cementum is less mineralization than root dentin. Biochemical analysis have revealed chondroitin 4-sulphate.

9%. areas of increased calcium concentration are indication of incipient carious lesion. Its concentration is highest in cementum amongst all calcified tissue. d. MAGNESIUM: It is present in concentration of varying from 0.1 to 3 %. FLUORIDE: It is an important constituent of the cementum.
b. CARBONATES f. e. c. Fluoride level in acellular cementum is more than that of cellular cementum.9%.tissue fluids. They are arranged paralled to lone axis of collagen fibrils (Selvig 1969).9% is seen at cemento-enamel junction. 0. The concentration is higher in areas that are exposed to oral cavity. An important aspect of magnesium concentration is that it is the first element to reach to reach out in early carious lesions and since it is not significantly reabsorbed during remineralization.5-0. CITRATES
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. The concentration is found to be 0. SULFUR: Sulfur is also present in varying concentrations ranging from 0.5% is seen at the surface while 0.

b. f. c. e.
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. adhesion to the root surface & cell differentiation.MICROSCOPIC STRUCTURE OF CEMENTUM: CEMENTOBLASTS: a. The components of multilayered cells are more flattened and that of single cells are cubiodal. The more cuboidal cells are between 8-12 µm in diameter. These tends to become differentiated into cementoblasts as they invade. They may form a single or multicellular layer. which is a derivative of the cranial neural crest. their nuclei are centrally located in basophilic cytoplasm. Other extracellular matrix proteins that have been suggested to play role in cementoblast differentiation are non-collagenous proteins which are also found in bone. Recent ultrastructural studies & immuno-histochemical studies support the hypothesis that the cementoblasts origin from epithelial cells of Hertwig¶s epithelial root sheath (HERS) when they undergo an epithelial mesenchymal transformation. Differentiation: The fibrogenic cells of the dental follicle are either fibroblasts or mesenchymal cells. approach & align themselves along the external border of the dentin to form cementogenic layer. Numerous processes are extending from principle cell mass of the cementoblast. They are fewer in number but longer in cells engaged in cementogenesis. These features of cementum are similar to those of other collagen producinf cells to which they are derivatively related. It is well known or accepted that cementoprogenitor cells arise from the dental follicle proper which os ectomesenchymal origin ( Tencate 1971). d. High concentration of two major non-collagenous proteins² bone sialoprotein & Osteopontin have been detected on the tooth surface and it is suggested that bone sialoprotein might be involved in precementum chemoattraction. an extensive network of surrounding well developed Golgi system & ribosomes. Origin: Cementoblasts are cemento-progenitor cells which synthesis collagen & protein polysaccharide (proteoglycans) which make up the organic matrix of cementum. These cells contain mitochondria.

that are preferentially directed towards periodontal ligament. the cytoplasm is palely basophillic and nucleus is centrally located.
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. The cementocytes cell body & its processes occupy lacunae & canaliculi respectively. The processes remain independent. These located in spaces termed lacunae. Nearly 30 such processes may project a single cell body. this is how cementocytes derive their nutrition from periodontal ligament and contributes to the vitality of this mineralized tissue. They may be 1µm n diameter & 15 µm in length. diameter ranges from 8-15 µm. Further while adjacent canaliculi of neighbouring cells communicate frequently. which are indistinguishable from osteoclasts. oval or squamoid. In the apical third cementoblasts during cementogenesis gets separated from its layer and are trapped in rapidly calcifying cemental matrix.
CEMENTOCLASTS: These are multinucleated giant cells. Golgi apparatus. A process & functional destiny similar to that of osteoblasts to osteocytes. The central mass may appear rounded. Cementum that is formed rapidly generally processes wider lamellae & more cementocytes.CEMENTOCYTES:
rd The apical one half or of root covers with cellular cementum. and have numerous cytoplasmic processes coursing in canaliculi. They are responsible for root resorption that leads to primary teeth exfoliation and is also in permanent dentition in mesial surfaces in compliance with mesial migration and may occur with occlusal trauma & orthodontic therapy. endoplasmic reticulum. These separated Cementoblasts differentiate into cementocytes. Extending from the surface of the cells are numerous protoplasmic processes. The morphologic & dimensional aspect of cementocytes is variable. mitochondria are similar quantitatively to those of osteocytes.
The number in cementocytes in the matrix is variable. Thus the metabolites progress mostly by diffusion through the canaliculi of cellular cementum.

is more irregular & contain cells (cementocytes) in individual spaces (lacunae). According to location on teeth (Kronfeld 1938): j Radicular cementum ± found on the root surface. except in a 10-50 µm wide zone near cemento-enamel junction where they are only partially calcified. Cellular cementum is less calcified than acellular cementum. Most fibers are inserted at approximately right angles into the root surface. cells that form it remain on its surface). It is the first formed cementum. Sharpey¶s fibers are completely calcified with mineral crystals oriented parallel to the fibrils. On the basis of cellularity (Gottlieb 1942): j Acellular cementum (Primary cementum) j Cellular cementum (Secondary cementum) ACELLULAR CEMENTUM: Refers to cementum lacking embedded cells. CELLULAR CEMENTUM: It is formed after tooth reaches the occlusal plane. Sharpey¶s fibers occupy a smaller portion of cellular cementum and are separated by other fibers that arranged either parallel to the root surface or at random. This cementum is formed before tooth reaches the occlusal plane and its thickness ranges from 30-230µm (Schroeder 1986). Acellular cementum also contains intrinsic collagen fibrils that are calcified and are irregularly arranged or parallel to the surface (Schroder 1980). B. parallel ~ 12 ~
. Both cellular & acellular cementum is arranged in lamellae separated by incremental lines. The thickness of cellular cementum is greater than acellular. covers approximately the cervical third or half of the root and does not contain cells. (i. Sharpey¶s fibers make up most of the structure of acellular cementum.e. which has a principle role in supporting the tooth. j Coronal cementum ± cementum that forms on the enamel covering the crown.TYPES OF CEMENTUM (CLASSIFICATION): A.

Its thickness is about 1 to 15 µm.5-3 µm / year) as long as the adjacent periodontal ligament remains undisturbed. They exhibit fibroblastic characteristics. but not yet mineralized.
2) Acellular Extrinsic Fiber Cementum (AEFC): It is composed almost entirely of densely packed bundle of sharpery's fiber and no cells. extend cell processes into an unmineralized dentin. ~ 13 ~
. It is a product fibroblasts and cementoblasts. & deposit collagen fibrils within it so that dentin & cementum fibers intermingle. These lines represent rest period in cementum formation & are more mineralized than the adjacent cementum (Romanos 1992). Acellular extrinsic fiber cementum continues to grow in thickness (@ 1. These are known as incremental lines of salter. 1) Acellular afibrilar cementum (AAC) 2) Acellular extrinsic fiber cementum (AEFC) 3) Cellular intrinsic fiber cementum (CIFC) 4) Cellular mixed stratified cementum (CMSC) 5) Acellular intrinsic fiber cementum (AIFC)
1) Acellular afibrilar cementum (AAC): Contains neither cells.to the long axis of the root. nor extrinsic or intrinsic fibers. Its thickness is between may extend further apically. Cementoblasts that produce AEFC differentiate in close proximity to the advancing root edge. During root development the first cementoblasts align along the newly formed. It is found in the cervical third of roots in human but may extend further apically. mantle dentin surface. apart from a mineralised ground substance. Schroeder (1986) has classified cementum again in five sub types bases on the presence of cells and organisation of collagen fibers. Its thickness is between about 30 to 230 µm. It is a product of cementoblasts and is found as deposited on the enamel over small areas of the dental crown just coronal to the cemento enamel junction.

1-0. The overall degree of mineralization of this cementum is about 45-60%. (Schrvederr 1986). These cells also secrete non collagenous matrix proteins that fill in the spaces between the collagen fibers. under the influence of non-collagenous matrix proteins. Therefore the collagen is of local or intrinsic origin. its initial part should be classified instead as having intrinsic fibers. AEFC develops slowly as the tooth is erupting. X-ray examination reveals that the innermost layer is less mineralized. the intrinsic fibrous fringe become connected to the PDL fiber bundles. CIFC is deposited on unmineralized dentin surface near the advancing root edge. 30. It appears primarily in the apical third of the roots & in furcation areas.5 µm/ year. It is formed by cementoblast and in humans it fills resorption lacunae meaning it¶s a form of resorptive cementum. once the tooth is in occlusion. a more rapidly formed & less mineralized variety of cementum.Mineralization of the mantle dentin starts internally & does not reach the surface until mingling has occurred. establishing cementodentinal junction. is a reflection of its significance. 3) Cellular mixed stratified cementum: It contains both collagen fibers & calcified matrix. Cementoblasts then migrate away from the surface but continue to deposit collagen so that a fine fiber bundle lengthens & thickens. 4) Cellular Intrinsic Fiber Cementum: It contains cells but no extrinsic (Sharpey's) fibers. Initially AEFC consists of mineralized layer with a short fringe of collagen fibers implanted perpendicular to the root surface. Although this cementum is classified as AEFC. It is deposited @ 0. This cellular mixed fiber cementum consists of AEFC and CIFC that alternate and appear to be deposited in irregular sequence upon one another (Schroeder 1993). It can repair a resorptive defect of the root in a
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. It is the co-product of cementoblasts & fibroblasts and consists of both extrinsic & intrinsic fibers. Only after the first 15-20 µm have formed. The extraordinary high numerical density of fibers inserting into AEFC (approx. as the collagen matrix of the first formed cementum results from cementum-associated cells & it¶s elaborated before the periodontal ligament forms. Mineralization then spreads across into cementum. AEFC has the potential to adapt to functionally dictated alterations such as mesial tooth drift.000/mm2).

Between the ages of 11 and 70 the average thickness increases threefold with the greatest increase in the apical area. This may occur in the furcation and on the apical root portions. 4. It is thicker in distal surfaces than in mesial surfaces probably because of functional stimulation from mesial drift over time (Polson A et al 1990).
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. ii. 3. 2. 1. slow deposition rate so that cells are not engulfed in their matrix and that forms without leaving cells behind (Bosshardt & Schroeder 1990). Distinguishing between fine based. iv. The thickness of cementum on the coronal half of the root varies from 16 to 60 µm or about the thickness of hair.densely packed intrinsic fibers running parallel to the root surface and larger. Inclusion of cementocytes within lacunae with processes directed towards the tooth surface.
Cellular intrinsic fiber cementum is initially deposited on root surface areas where no acellular extrinsic fiber cementum has been laid down on the dentin. THICKNESS OF CEMENTUM & ITS CLINICAL SIGNIFICANCE: Cementum deposition is a continuous process that proceeds at varying rates throughout life. In the light microscope CIFC is identified easily because of i. In the apical third and furcations the thickness is highest up to 150 to 20 µm.reasonable time due to its capacity to grow much faster than any other known cementum type. Average thickness of 95 µm at age 20 and 215 µm at age 60 have been reported (Zander HA 1958). iii.e. Its laminated structure. 5) Acellular Intrinsic Fiber Cementum: It is an acellular varient of cellular intrinsic fiber cementum that is also deposited during adaptive responses to external forces i. Presence of cementoid on its surface. haphazardly incorporated extrinsic fibers running at right angles to the root surface.

In deciduous teeth C-D junction is sometimes scalloped or wavy. They encountered numerous tiny cytoplasmic processes into loosely arranged & not yet mineralized dentinal matrix. TYPES OF JUNCTIONS & ITS CLINICAL SIGNIFICANCE: a. The dentin surface upon which cementum is deposited is relatively smooth in permanent teeth. In such preparation cementum usually stains more intensely than does dentin.Cementum formation is most rapid in apical regions where it compensated for tooth eruption which itself compensates for attrision. it does not exhibit characteristic feature of either of dentin or cementum. This layer is rich in glycoprotein but contains sparsely distributed collagen fibrils. In certain teeth near cemento-dentinal junction an ill-defined zone called intermediate cementum is found. It is frequently observed between acellular extrinsic fiber cementum and dentin (Orban 1952). The crucial step leads eventually to an intimate interdigitation of the two different fibrils populations. ~ 16 ~
. while those of dentin are arranged somewhat haphazardly. Recent studies by Inamoto et al have suggested that mucopolysaccaharides might have an important role in cemento-dentinal junction formation. This view is based on the fact that fibril interdigitation is not uniform along the length of junction and moreover. CEMENTO-DENTINAL JUNCTION: After differentiation of cementoblats extend numerous tiny processes at the beginning of their maturation on the root surface. The mineralization in dentin does not reach the future dentino-enamel junction until the dentinal matrix is covered with collagen fibrils of cementum. This zone contains cellular remnants of HRS embedded in a calcified ground substance (Lester 1969). This layer is predominantly seen in the apical rd of roots of molars & premolars. In decalcified preparations cementum is more electron dense than dentin and some of its collagen fibrils are arranged in relatively distinct bundles. on application of hyaluronidase there is a split in the junction and there is no effect of this enzyme on collagen fibrils but they do have an effect on mucopolysacchrides. The interface between cementum and dentin is clearly visible in decalcified and stained histologic sections using the light microscope. The attachment of cementum to dentin is quite firm.

In such cases the width of cementum overlying enamel increases. y The cementum at and immediately subjacent to the CEJ is of particular importance in root planning procedures. reticular material termed afibrilar cementum. y In about 10 % of cases. fibrilar cementum with characteristic 64nm (640 A0) periodicity is deposited. 2) Apical cementogenesis compensates for attrition of enamel tips and edges thereby maintaining occlusal functional relationship. cementum overlaps the cervical end of enamel for a short distance. CEMENTO-ENAMEL JUNCTION: The relation between cementum and enamel at the cervical region of teeth is variable y In about 30% of all teeth cementum meets the cervical end of enamel in a relatively sharp line. This is called afibrilar cementum¶ because it lacks the characteristic 64nm periodicity of collagen fibers. y In approximately 60 % of cases. it should be noted that if such cementum is allowed to 5remain in contact with connective tissue for sufficiently long time.
FUNCTIONS OF CEMENTUM: 1) Anchorage: The primary function of cementum is to furnish a medium for the attachment of collagen fibers that bind tooth to alveolar bone. electron dense. enamel and cementum do not meet. However. y This occurs when the enamel epithelium degenerates at its cervical termination permitting the enamel to come in direct contact with the connective tissue to produce a laminated. 4) Also provides for fiber reattachment and relocation due to mesial drifting of teeth. Presumably this occurs when the enamel epithelium is delayed in its separation from dentin.b. In such cases there is no cemento-enamel junction. 3) Assist in maintenance of width of the periodontal ligament by cementogenic activity. ~ 17 ~
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8 % of these areas were found to be present in apical third. In the postertior teeth cementum is thicker on distal side than mesial.5.5) Serves as a major reparative tissue for root surface. In a microscopic study average number of resorption areas per tooth was 3. Damage to root surfaces such as fractures and resorption can be repaired by deposition of new cementum. RESORPTION: Although physiological root resorption is a normal phenomenon of deciduous teeth during tooth shedding. 2. Thicker layers of cementum may form in root surface grooves and in the furcations of multirooted teeth.
AGE CHANGES: 1. The cementum of erupted as well as unerupted teeth is subject to resorption. DEPOSITION: Cementum formation on the roots of human teeth is continuous throughout life unless disturbed by peripical or periodontal pathology. The resorptive changes may be of microscopic proportion or sufficiently extensive to be visible on a radiograph. permanent teeth do not undergo physiological resorption. Nonfunctioning. Cementum resorption is extremely common. The distribution of cementum on impacted teeth tends to indicate that occlusal forces are not necessary to stimulate cementum deposition. Also great variations in width of incremental layers indicate that the rate of cementum formation may vary from time to time. sharpey's fibers may be nearly completely absent and the cementum is built up mainly by intrinsic fibers arranged parallel to root surface (Imgruth 1959). 76. 19. indiacating a relationship to mesial drift (Polson A 1990). impacted teeth generally appear to have thicker cementum than functioning teeth (Azaz B 1974). 6) Protecting underlying dentin. More cementum is formed apically than cervically. In the cementum of impacted teeth.
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.2% in middle third and remaining 4 % in coronal third (Henry 1951).

Calcium deficiency. cyst. Hereditary fibrous osteodystrophy.Microscopically. tumor. And Non pathologic: 1. Although it is widely accepted that the root surface is more resistant to resorption than alveolar bone. 4. Replanted and transplanted teeth. In the vast majority of cases idiopathic resorption does occur (Massler et al 1954). (Massler1954). Hypothyroidism. Systemic conditions ± 1. Pressure from misaligned erupting tooth. Embedded teeth. Trauma from occlusion. 3. it is also known that the number of teeth resorbed and the severity of resorption are markedly increased by orthodontic treatment. REPAIR: Cementum resorption is not necessarily continuous & may alternate with periods of repair & deposition of new cementum. Periapical diseases. Periodontal diseases. cementum resorption occurs as bay like concavities in the root surface.
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. 2. Reversal line contains a few collagen fibrils & highly accumulated proteoglycans with mucopolysaccarides. Multinucleated giant cells and large mononuclear macrophages found adjacent to cementum undergoing active resorption Causes may be local or systemic or may occur without any apparent etiology. 3. 2. 2. Local causes ± May be pathologic: 1.
3. Root resorption can be further classified by location into internal and external and by the degree of persistence into transient or progressive. Orthodontic tooth movement. Newly formed cementum is demarcated from root by a deeply staining irregular line termed as a reversal line which delineates the border of the previous resorption. 3.

It occurs most frequently in the primary dentition (McNamara et al 2000). Saygin et al (2000) suggested that epithelial cell rests of Malassez may be related to cementum repair by activating their potential to secrete matrix proteins such as amelogenins. Hasegawa et al (2003) stated that epithelial cell rests of Malassez are the only odontogenic epithelial cells in the periodontium after eruption and they may have some function in repair & regeneration under specific conditions. 4. If epithelium proliferates in resorption area. Ankylosis may also develop after chronic peri apical pathology. enamelins & sheath proteins. Cementum repair requires viable connective tissue. Cementum formation is critical for appropriate maturation of the periodontium both during development & regeneration. occlusal trauma & around embedded teeth. eruption as well as ability of teeth & periodontium to adapt to altered force levels or direction of force is greatly reduced. It ~ 20 ~
. ANKYLOSIS: It is the fusion of the cementum & alveolar bone with obliteration of PDL. Clinically ankylosed teeth lack physiologic mobility of normal teeth which is one of the first diagnostic sign for ankylotic resorption. which suggests that it may represent a form of abnormal repair. An embedded fiber of PDL establishes a functional relationship in a new cementum. tooth replantation. Fuss Z (2003) suggested that these teeth usually have a special metallic percussion sound & if the ankylotic process continues. 5) EXPOSURE TO ORAL ENVIRONMENT: Cementum becomes exposed to oral environment in gingival recession & as a result of loss of attachment in pocket formation. Ankylosis results in resorption of root & its gradual replacement by bone tissue. repair will not take place. Proprioception. inorganic ions & bacteria. they will be in infraocclusion. Cementum is sufficiently permeable to be penetrated by organic substances. For this reason reimplanted teeth that ankylose will loose their roots after 4-5 years and will be exfoliated. physiologic drifting. It occurs in the teeth with cemental resorption.

CHANGES IN PERIODONTIUM DURING POCKET FORMATION: Periodontal pocket is defined as pathologically deepened gingival sulcus. root caries.e. sometimes leading to pulpal pathology. Increase mineralization does not come from adjacent areas. B) Chemical changesThe exposed cementum has increased mineral content (Selvig 1966). The following minerals are seen in increased concentration. exposure to oral cavity of minerals and organic component at the cementum ± saliva interface. These are probably a result of exchange on. A] Structural changesa) Presence of pathologic granules: These may represent areas of collagen degeneration or the areas that have not been fully mineralized initially (Bass 1951). sensitivity to sweets and thermal changes or severe pain. Ca. The root surface wall of periodontal pocket often undergoes various changes that are significant because they may perpetuate the periodontal infections. chemical or cytotoxic. The changes may be grouped as structural. These may lead to pulpitis. root caries etc.leads to hypersensitivity to thermal changes or tactile stimulation. Mg. as there is no zone of demineralized areas nearby. As a result there is softening of cementum and it may undergo fragmentation and cavitations i. F. P.
b)
Areas of increased mineralized mineralization: (Selvig 1966) These are areas seen as layer of 10 ± 20 Qm thick. Exposed ~ 21 ~
. although the areas may be as thick as 50Qm thick. cause pain and complicate the periodontal treatment. Pathologic pulpal exposure occurs in severe cases. Theses hyper mineralized area is associated with increased crystal perfection.
c)
Areas of demineralization: Exposure to oral fluid and bacterial plaque results in proteolysis of the embedded remnant of sharpey¶s fibers.

However when the forces exceed cementum resorption occurs on pressure side and cementum deposition takes place on tension side.e. II) Cementum changes during orthodontic movement: Orthodontic movements when in proper magnitude don¶t affect the cementum because cementum with its slow metabolism is not damaged by a pressure equal to that exerted on bone. III) Fracture of the root: Cementum is repaired by deposition of new cementum. Cementum repair requires the presence of new viable connective tissue. Cementum repair can occur in non-vital as well as vital tooth. repair will not take place. reduced cementum formation. Deficiency in alkaline phosphatase characterized by premature loss of primary teeth. No co-relation has been established between occlusal function and cementum deposition.cementum may absorb a highly calcified layer i.
LOCAL CONDITIONS LEADING TO CHANGES IN CEMENTUM:
I) Changes in cementum in TFO:
Cementum deposition continues after teeth have reached into contact with their functional antagonists and throughout life. if epithelium proliferates into that area. In addition bacterial products such as endotoxins are also found deep in cementum wall of periodontal pocket. However cementum has been found to be thinner in cases of increased forces as well as thickening in some cases also been reported. resistant to decay. C) Cytotoxic changesThese include bacterial penetration into cementum as deep as CDJ. This ability of cementum to absorb materials are toxic. ~ 22 ~
. IV) Cementum Hypophosphatasia: Hypophosphatasia is caused by mutation in tissue specific alkaline phosphatase gene.

In some patients serum alkaline phosphatase is abnormally low. Severally affected individuals do not survive beyond childhood. the permanent incisors & first molars show advanced pocket formation. In the familial form of LJP. Cementum formation on the primary anterior teeth is usually defective. A decreased efficiency of neutrophil response to periodontal pathogens has also been reported in patients with LJP. Other skeletal abnormalities are also present. A study showed a paucity or complete absence of cementum due to defective formation of cellular cementum on both erupted and unerupted teeth (Ruston MA 1956) Prolonged retention of deciduous teeth. 3. Premature loss of teeth without root resorption is one of the first signs of the disease. subsequent delayed eruption of succedaneous teeth as well as numerous unerupted supernumerary teeth also seen.It is hereditary disease transmitted as an autosomal recessive trait. Individuals with this condition shows dwarfism but have relatively well proportioned body. 2. Low levels of alkaline phosphatase leads to defect in formation & mineralization of cementum. This condition primarily affects the skull. Cemental hypoplasia occurs on root surface of patients suffering from hypophosphatasia. The pathogenesis of tooth loss in these two diseases underscores the importance of normal values of alkaline phosphatase during periods of root development. tissue destruction develops rapidly without an associated inflammatory process. clavicle and dentition. In adolescents it resembles localized juvenile periodontitis (LJP). Hypopituitarism :In hypopituitarism there is reduced recreation of pituitary hormones specially GH. Root surface of the affected teeth have hypoplastic cementum. In patients with LJP.
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. Papillon Lefevre syndrome:It is a familial. characterized by aggressive periodontitis with early loss of deciduous as well as permanent teeth. loss of attachment and advanced alveolar bone resorption. Decreased cementum formation is associated with hypopituitarism. autosomal recessive disease. SYSTEMIC CONDITIONS LEADING TO CHANGES IN CEMENTUM: 1. Cleidocranial dysplasia:It¶s a developmental anomaly affecting mainly skeleton and teeth.

it is termed a cementum hypertrophy. This condition frequently is found in teeth that are exposed to great stress. Hypothyroidism :Eruption rate is delayed. It may be localized to one tooth or effect the entire dentition. deciduous teeth retain beyond their normal shedding time. It the over growth improves the functional qualities of the cementum. 5. Treatment lies in extraction of tooth along with complete removal of growth. It also appear in the form of spike like excrescences created by either the coalescence of cementicles that adhere to root or the calcification of periodontal fibers at site of insertion into the cementum (Lester 1969. It occurs as a generalized thickening of cementum with nodular enlargement of apical third of root. it is termed hyperplasia. Mandible is threefold more commonly affected then maxilla. Lesion is slow growing and usually asymptomatic. Hyperthyroidism :Shedding of deciduous teeth earlier n eruption of permanent teeth is greatly accelerated. Down¶s syndrome:NEOPLASM OF CEMENTUM:Benign Cementoblastoma is a true neoplasm of functional Cementoblasts that form large masses of cementum like masses on root surface (Farman 1979).4. HYPERCEMENTOSIS: It refers to prominent thickening of cementum. The lesion normally occurs under the age of 25 years with no sex predilection. CEMENTAL ABBERATIONS:i. If the overgrowth occurs in nonfunctional teeth or if it¶s not correlated with increased function. In localized hypertrophy a spur or prong like extension of cementum may be formed.
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. 6. Recurrence is uncommon and is seen in few cases that are attributed to incomplete removal of the cemental mass. Radiographically it appears as a dense radio opaque mass often surrounded by thin radiolucent line.

ii. radio-opaque mass in which isolated radiolucent markings may be seen. They too develop around degenerated epithelial rests. Hyperpituitarism. y Teeth without functional antagonist as an attempt to keep pace with excessive tooth eruption. y In low-grade periapical irritation from pulp disease it compensates for destroyed fibrous attachment to tooth. These develop from calcified epithelial rests. y Excessive tension from orthodontic forces. Cementoma occurs more frequently in females than males. here the hyperplasia is circumscribed and surround the root like a cuff. y Non-functional teeth. (Gigantism and Acromegaly) (Sponge 1979).2 mm.The prong like extensions of cementum provide a longer surface area for the attaching fibers. from calcified sharpey¶s fibers and thrombosed vessels within the PDL.
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. Sometimes embedded calcified round bodies frequently are found in localized areas of hyperplastic cementum such knoblike projections are designated as excementosis. Radiographically the lesion appears as discrete. Etiology is varied is not completely understood. They are seen more commonly in mandible as compared to maxilla and may be single or multiple. The diameter of individual cementicle rarely exceeds 0. Extensive hyperplasia of cementum is occasionally associated with chronic periapical inflammation. around small spicules of cementum or alveolar bone traumatically displaced into PDL. dense. They are considered either odontogenic neoplasm or developmental malformations. thus the firmer anchorage of the tooth to the surrounding alveolar bone is assured. CEMENTICLES: Calcified bodies in the PDL that are adherent to or detached from the root surface. y Excessive occlusal forces.
iii. y Paget¶s disease. CEMENTOMA: These are masses of cementum generally situated apical to teeth to which they may or may not be attached. osteitis deformations.

Regeneration. Removes smear layer. Citric acid produces 4µm deep demineralized zone with exposed collagen fibers. enamel & dentin matrix into muscle tissue of animals induced mesenchymal cells to differentiste into osteoblasts & started osteogenoc process. Lactic acid and EDTA). Citric acid: studies by Urist (1965) showed that implantation of demineralized bone. exposing dentinal tubules. repair and new attachment are the aspects of periodontal healing that have a special bearing on the results obtainable by treatment. Root conditioning can be done by using acids (citric acid. 1. Acid demineralization: The teeth treated with acid demineralization heal by connective tissue reattachment. Fibronectin and EMP. HCL. enlarges the opening of dentinal tubules and exposes the collagen dentinal matrix. Detached cementum may be reunited by new cementum formation or may be completely resorbed or undergo partial resorption followed by addition of new cementum and embedding of collagen fibers. It removes dentinal smear layer. wider with funnel shaped orifices. ~ 26 ~
. root planing or root conditioning is a necessary antecedent to mesenchymal cell migration & attachment onto the exposed root surface. The detachment may be complete or incomplete.iv. Following actions of citric acid have been reported: Accelerated healing & new cementum formation.
CEMENTAL TEARS: Detachment of fragments of cementum from root surface is known as cemental tear.
CHANGES IN CEMENTUM DURING DIFFERENT PERIODONTAL THERAPY: Mechanical and chemical means have been used to promote favorable root surface characteristics. Eliminate endotoxins & bacteria from the diseased tooth surface. This exposed matrix provides substrates for fibrin linkage and can support attachment and migration. A) ROOT BIOMODIFIERS:It is well accepted that in order to improve periodontal healing. with evidence of accelerated cementogenesis.

7 for 15 seconds. The view is based on finding that cells of HERS deposit EMP on the root surface. y Apply cotton pledges soaked in saturated solution of citric acid (pH 1. done preferably under LA. The faster reattachment might be the result of opsonization in root bound endototoxins 4. y Replace the flap n suture it. calculus and / or any other plaque retentive factors. Fibronectin: It is a multifunctional high molecular weight glycoprotien involved in cell adhesion and attachment of cells to their surrounding matrix.Recommended citric acid technique is as follows:y Raising mucoperiosteal flap. Through root planing of diseased root surface. to modify the root surface provides no clinical significant benefit for regeneration in patients with chronic periodontitis.0) for 2-5 mins. various root surface changes occurs due to bacterial deposits on the root surface. Therefore to remove these from root surface basic treatment modality in any type of periodontitis is Root planing. EDTA etc. Rylander root planing is defined as technique of instrumentation by which the soften cementum is removed & root surface is made hard & smooth and can be performed as either closed or open approach. According to Jan Lindhe & H. Objectives of root planing:. 2. It is applied on the root surface in the concentration of 24% at the pH of 6. y Remove cotton pledges & irrigate root surface profusely with water. B) ROOT PLANING:In periodontitis. 3.(Walter Cohen & Lindsey Sherwood)
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. EMP: Application of EMP (amelogenins) may promote periodontal regeneration because it mimics the events that took place during the development of periodontal tissues. EDTA (Ethylene-diamine-tetra acetic acid):It is also used as citric acid to remove smear layer. It provides faster reattachment. However systemic review by Mariotti (2005) suggested that the use of citric acid. arrest of disease progression & removal of the nidus of infection from the area is performed. thoroughly instrument the root surface.

Shrinkage of deepened pathologic pocket to a shallow healthy gingival sulcus. superficial demineralization subsequently remineralizes from adjacent tissue fluid 2-3 days after surgery. epithelial attachment. . . New dentogingival junction forms within 2 weeks. gain in clinical attachment.Providing root surface compatible with reestablishment of healthy connective tissue.Suppression or elimination of pathogenic periodontal microflora & replacement with sparse flora found in health. Mechanism of binding together of these hard tissues is essentially same for AEFC & CIFC: Mineralization of mantle dentin starts internally & does not reach surface until collagen fibrils of dentin & cementum had time to blend together. It is necessary to prepare root surface to the extent that mineralized dentin / cementum is exposed at the time of surgery. once layer gets mineralized. This is because of acid & enzymatic activity of post surgical inflammation. . After root planing response of the periodontium occurs as a result of reduction in probing depth..
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. Frank & Cimanosi stated that remineralization of this layer occurs soon after deposition of new cementum external to the dentin. HOW DOES CEMENTUM HOLD ONTO DENTIN? Attachment mechanism of cementum to dentin is both biological interest and of clinical relevance since pathological alteration & clinical intervention may influence the nature of exposed root surface & hence the quality of new attachment that forms when repair cementum is deposited. Ruben et al 1975 suggested that the therapeutically debrided & planed root surface initially undergo superficial demineralization & resorption of the cemental matrix that involves embedded collagens & reticular fibers. Cementoblasts comes from PDL & undifferentiated mesenchymal cells.Conversion of inflamed. bleeding or suppurative pathologic pocket to healthy gingival tissue. occurs 48hrs after surgery. cementogenesis takes place.

Resulting in amalgamated mass of minerals. and new attachment are aspects of periodontal healing that have a special bearing on the results obtainable by treatment. An undifferentiated connective tissue cell develops into osteoblasts and cementoblasts. but by connective tissue which is the precursor of both. attachment and proliferation and proper phenotypic expression of periodontal connective tissue progenitor cells. Bone and cementum are not replaced by existing bone and cementum. Then it spreads through surface layer of dentin.
CURRENT CONCEPTS DURING PERIODONTAL REGENERATIONS: CHANGES OR HEALING AFTER PERIODONTAL THERAPY: The process of PDL tissue regeneration starts at the moment of tissue damage. Regeneration: It is the growth and differentiation of new cells and intercellular substances to form new tissues or parts. Repaired cementum adheres very well to root surface if a resorptive phase precedes new matrix deposition (Bosshardt DD 2005). repair. A critical step in periodontal regeneration therapy is to alter the periodontitis affected root surface to make it a hospitable substrate to support and encourage migration. which forms bone and cementum. Periodontal treatment ~ 29 ~
. Regeneration. . by GF &N cytokines released by damaged CT & inflammatory cells. Continuous deposition of cementum takes place by (removing bacterial plaque and calculus and) creating the conditions that enhances its new formation.implying that the odontoblasts favorably precondition the root surface. Regeneration takes place by growth from the same type of tissue that has been destroyed or from its precursors. across dentin-cementum junction & into cementum. From biochemical perspective this arrangement appears optimal for strong union between dentin & cementum.

But the 2nd intervention to remove it was required so the second generation of guided tissue regeneration used absorbable membranes made of collagen or polylactic and citric acid (Miller et al 1996) which eliminated the need for surgical membrane retrieval. et al 1997). Excluding gingival epithelium & gingival connective tissue from root surface during the post surgical healing phase not only prevents epithelial migration into the wound but also favours repopulation of the area by cells from the pdl & bone. Studies on experimentally induced periodontal defects in monkeys suggested that guided tissue regeneration was capable of inducing the formation of new bone and cementum (Amar S. New Attachment:New attachment is the embedding of new periodontal ligament fibers into new cementum and the attachment of the gingival epithelium to a tooth surface previously denuded by disease.(1982) using Millipore® membranes. thus temporarily separating them from the gingival epithelium. The first guided tissue regeneration membranes were nonabsorbable and made of polytetrafluoroethylene. ~ 30 ~
. Nyman et al. introduced the concept of a membrane barrier. such as Gore-Tex®. which excludes the apical migration of gingival epithelial cells and provides an isolated space for the inwards migration of periodontal ligament cells.
GUIDED TISSUE REGENRATION: The method for prevention of epithelial migration along the cemental wall of the pocket. Repair: Restoration of destroyed periodontium involves mobilization of epithelial and connective tissue cells into the damaged areas and increased local mitotic divisions to provide sufficient number of cells.removes the obstacles to regeneration and enables the patient to benefit from the inherent regenerative capacity of the tissues. osteoblasts and cementoblasts. GTR consists of placing barriers of different types o cover the bone & pdl.

It has also been questioned whether guided tissue regeneration produces true cementum regeneration or only cemental repair. which will result in a regenerated cementum similar to pristine cementum as maturation proceeds over time (Graziani F et al 2005). In contrast. transient root resorption/demineralization..
DO ENAMEL ± ASSOCIATED PROTEINS GENERATE CEMENTUM. This matrix apparently is produced by cementoblasts like cells that occasionally are embedded in their products as cementocytes. Slavkin (1989) stated that based on the presence of enamel proteins in acellular cementum. In the first pattern. Hammerstrom (1997) tested this idea by adding enamel proteins or purified enamel matrix derivative to surgically produced periodontal defects in monkeys followed ~ 31 ~
. ii. but not for intrabony defects. running both axially & circularly. The newly formed cementum has been characterized as a cellular cementum that is usually poorly attached to the dentin surface (Kostopoulos L et al 2004). The 1st stage comprises an initial healing phase with the formation of a blood clot. It is suggested that periodontal healing with guided tissue regeneration therapy occurs in two stages. a fringe of collagen fibrils oriented more or less perpendicular to the pre-existing root surface is laid down initially. This fringe seems to be formed by cells resembling cementoblasts. The use of grafting material in combination with guided tissue regeneration seems to improve clinical outcomes for furcation. The 2nd phase comprises a remodeling process. Under the guided conditions used. deposition of acellular cementum on the root surface and formation of connective tissue. electron dense material & apparently lack an attachment to dentin characterized by inter-digitations of collagen fibrils as seen along natural CDJ. 2nd pattern of regeneration involves the accumulation of sheets of collagen fibrils arranged largely parallel to the root surface. cementogenesis follows atleast two distinct patterns:i.?? Lindskog (1982). Both the types of regenerative cementum seem to merely adhere to the supporting hard tissues through an intervening thin layer of afibrilar. it was thought that these proteins may play a role in the repair/regeneration of periodontal tissues destroyed by periodontal disease.

which has been marketed by Biora. the use of enamel proteins for inducing the formation of cementum. available data suggest an increased migration of periodontal ligament cells. however Tokiyasu et al (2000) found decreased mineralization of cementoblast cells and inhibited the mineralization of dental follicle cells. osteoblasts. taken together. Nevertheless.by histological analysis that showed almost complete regeneration of acellular cementum. bone and dentin has generated numerous in vivo and in vitro studies. under the name of Emdogain®. increased mineralization of osteoblasts and gingival fibroblasts. In the past 8 years. and can ~ 32 ~
. However. Similarly most studies on the effect of EMD on cell attachment. consisting of hydrophobic enamel matrix proteins extracted from porcine developing enamel. In vitro studies. as well as clinical trials. These studies resulted in a new therapeutic preparation to treat periodontal disease. have found an increase in cell proliferation in the presence of EMD. firmly attached to the dentin and with collagenous fibers extending towards newly formed alveolar bone. A number of studies.. it was found that EMD induced mineralization of periodontal ligament cells. which measured the effect of EMD on cell proliferation. these studies suggest that enamel matrix derivative can act as a multipurpose growth factor capable of stimulating the proliferation of mesenchymal cells while inhibiting the cell division of epithelial cells. Hammerstrom (1997) stated that application of EMD suppresses the down-growth of junctional epithelium onto dental root surfaces. resulting in almost 300 publications. When mineralization was measured. with the exception of one study by Palioto et al (2004) that found no effect on periodontal ligament cells. animal studies and clinical trials are all being conducted simultaneously. which generally included periodontal ligament cells. Inc. Differences in results amongst studies can be explained by differences in sources and concentrations of enamel matrix derivative and in the cell preparations used. gingival fibroblasts and dermal fibroblasts in response to enamel matrix derivative. Several studies have tested the effect of enamel matrix derivative (EMD) on cell migration. found an increase in cell attachment. a process that frequently interferes with the formation of new connective tissue attachments. in few studies by Vander pau (2000) Davenport (2003) did not find this proliferative effect.

both groups showed good fill of the osseous defects studied. suggesting the presence of more than one growth factor. It has long been recognized that a recolonization of periodontal ligament cells onto the root surface is necessary for periodontal ligament regeneration. and then to cover the area with an artificial basement membrane. and that the action of enamel matrix derivative is mediated by the smad. Therapeutic approach proposed by Terranova et al (1990) is the removal of autologous cells from the patient¶s periodontal ligament. After 6 months. using hydroxyapatite as a vehicle for cell delivery. Studies by Kawase et al (2002) demonstrated that porcine enamel matrix derivative contains transforming growth factor-b1 (or a transforming growth factor-b-like substance). periodontal ligament and alveolar bone has also been observed by Kawaguhi (2004) using auto-transplantation of bone marrow mesenchymal stem cells into periodontal osseous defects in dogs. the treated patients exhibited greater pocket reduction and clinical attachment gain. Iwata et al (1998) isolated the inductive activity of enamel matrix derivative by using chromatography and characterized it as being BMP-2 and BMP-4 using specific antibodies. A pilot study was carried out by Hou LT et al (2003) with four patients. a neutralizing antitransforming growth factor-b immunoglobulin blocked the action of enamel matrix derivative on epithelial cells. in the presence of noggin (an inhibitor of BMPs). ~ 33 ~
.stimulate attachment and phenotypical changes in some cells. In addition. had an effect similar to that of amelogenin on periodontal ligament cells. and less gingival recession. indicating that BMPs are the molecules responsible for enamel matrix derivative activity. Studies by Maycock et al (2000) found that. Furthermore. however. enamel matrix derivative lost its inductive activity. another enamelassociated protein. while inhibiting matrix production in others. Regeneration of cementum. Emdogain®contains metalloproteases and serine proteases. Furthermore. although it failed to block completely enamel matrix derivative-induced fibroblastic proliferation. a post-translational modified recombinant ameloblastin. to place them back onto the exposed root coated with chemoattractant factors. culture of the cells in vitro. Emdogain® is made from an extract of enamel proteins. it is important to identify the actual protein responsible for its function.2 signaling pathway. than control patients. in addition to amelogenin.

Similar results have been observed by Akizuki (2005) after the application of periodontal ligament cell sheets. or their secreted products. The dynamic features of cementum are particularly highlighted by its repair potential. Chemical composition is approximate same as that of bone. By virtue of its structural dynamic qualities. non . cementum covering of the root increases in thickness throughout life.
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. faster apically than cervically. The discovery of a variety of non-collagenous proteins in cementum has apend a new research area of great therapeutic potential. Unless disturbed. provides tooth attachment and maintenance of occlusal relationship. Zeichner-David (2003) exploring the ability of these cells. Minor.pathological resorption defects on the root\ surface are generally reversible and heal by reparative cementum formation which obviously recapitulates developmental cementogenesis. So the application of cementum derived growth or attachment factors may result in accelerated wound healing and in controlled neocementogenesis following periodontal regeneration therapy. In diseased periodontium. which deposits two collagen containing varieties of cementum with completely different properties. to induce periodontal ligament cells to differentiate into cementoblasts in vitro. cementum may undergo alterations in structure as well as in the composition of its organic and inorganic components consequential to pathological changes. These multiple functions are fulfilled by the biologic activity and reactivity of cementoblast.
CONCLUSION: Cementum is a part of periodontal attachment apparatus.